ライフサイエンスコーパス: foam cell

1 ons after co-culture with macrophage-derived foam cells).

2 o promote cholesterol efflux from macrophage foam cells.

3 a newly characterized pathway in macrophage foam cells.

4 through the formation of macrophage-derived foam cells.

5 Hb), are devoid of neutral lipids typical of foam cells.

6 atory-response genes, observed in macrophage foam cells.

7 Eventually, they ingest lipids and become foam cells.

8 ated glucose uptake in human macrophages and foam cells.

9 inocytosis converting these macrophages into foam cells.

10 by macrophages converts the macrophages into foam cells.

11 good potency on cholesterol efflux in THP-1 foam cells.

12 ecause it did not transform macrophages into foam cells.

13 mation of lipid-laden THP-1 macrophages into foam cells.

14 nsformation of macrophages into E-LDL-loaded foam cells.

15 ibrous caps, large lipid pools, and abundant foam cells.

16 e cancers, is accompanied by the presence of foam cells.

17 y lipoproteins (LDLs), generating macrophage foam cells.

18 phagocytosis and efferocytosis in macrophage foam cells.

19 reby promoting the formation of inflammatory foam cells.

20 lated cholesterol is removed from macrophage foam cells.

21 efficient to promote the formation of hVSMC foam cells, a crucial vascular component determining the

22 , the hyperlipidemic mice exhibited numerous foam cells, a probable cause of increased swelling and p

23 ge IGF1R signaling suppresses macrophage and foam cell accumulation in lesions and reduces plaque vul

24 but rather induced a significant macrophage foam cell accumulation in murine atherosclerotic plaques

25 with respect to cholesterol efflux in THP-1 foam cells, albeit weaker in potency.

26 accumulation in macrophages and formation of foam cells, an early step in the development of atherosc

27 In vivo and in vitro foam cell analyses showed apoE-CD16 DKO macrophages accu

28 fect plaque-residing macrophages, potentiate foam cell and extracellular trap formation, induce endot

29 iate into macrophages and macrophage-derived foam cells and cause atherosclerotic lesions.

30 ly associated with cardiovascular disease in foam cells and clinical specimens from patients with AS.

31 tion of secondarily necrotic macrophages and foam cells and the formation of an advanced lesion with

32 associated with M1-polarized macrophages and foam cells and was experimentally induced during macroph

33 leukocyte accumulation, lipid accumulation, foam cells, and endothelial cell injury.

34 ent hyperlipidemic mice revealed accelerated foam-cell apoptosis, which subsequently led to the atten

35 yperlipidemic atherosclerosis by suppressing foam-cell apoptosis.

36 Foam cells are a hallmark of atherosclerosis.

37 Cholesterol-laden macrophage foam cells are a hallmark of atherosclerosis.

38 Inflammation and macrophage foam cells are characteristic features of atheroscleroti

39 tes, from which macrophages and most DCs and foam cells are derived, and reduce atherosclerotic lesio

40 Second, about half of all foam cells are smooth muscle cell-derived, retaining smo

41 established that cholesterol ester-enriched foam cells are the hallmark of atherosclerotic plaques.

42 Monocyte-derived foam cells are the hallmark of early atherosclerosis, an

43 Since foam cells are therapeutic targets in atherosclerosis, f

44 Macrophage-derived foam cells are thought to play a major role in atheroscl

45 Lipid-laden macrophages or "foam cells" are the primary components of the fatty stre

46 Lipid-laden macrophages, or foam cells, are observed in the lungs of patients with s

47 er ischemic injury, less swelling, and fewer foam cells at 3 d after ischemia.

48 uce an inflammatory response and deposits in foam cells at the atherosclerotic plaque, it also regula

49 open new avenues for an innovative anti-VSMC foam cell-based strategy for the treatment of vascular l

50 search on the disease-specific mechanisms of foam cell biogenesis and function is needed to explore t

51 cretion, and in human macrophages it induced foam cell biogenesis and M1 polarization.

52 cent studies indicate that the mechanisms of foam cell biogenesis during tuberculosis differ from tho

53 alveolar macrophages and macrophage-derived foam cells, both cell types relevant to tuberculosis pat

54 humans, whereas inflammatory macrophages and foam cells, but not circulating monocytes, are major leu

55 promotes cholesterol efflux from macrophage foam cells by directly up-regulating its key cellular me

56 to the plaque and impaired the formation of foam cells by enhancing cholesterol efflux from macropha

57 e may facilitate the formation of macrophage foam cells by impairing cholesterol efflux by the ABCA1

58 s in macrophages and its transformation into foam cells by increasing the expression of scavenger rec

59 ich necroptosis was induced in THP-1-derived foam cells by serum deprivation.

60 ple lines of evidence support that enhancing foam cell cholesterol efflux by HDL (high-density lipopr

61 contained a significantly elevated number of foam cells congesting the sinusoidal space, a feature co

62 In contrast, the size, foam cell content, and aortic pool size of iodinated LDL

63 oprotein (LDL) cholesterol-loaded macrophage foam cells contributes to the development of atheroscler

64 sm through which SCAP signaling affects VSMC foam cell development.

65 macrophages exhibit increased expression of foam cell differentiation markers including 15-lipoxygen

66 o promote cholesterol efflux from macrophage foam cells, direct experimental support for this hypothe

67 ony stimulating factor in splenic macrophage foam cells, driving BM monocyte and neutrophil productio

68 The varied behaviour of macrophages and foam cells during atherosclerosis and its clinical seque

69 n of excess cholesterol, as well as improves foam cell efferocytic function.

70 pported in part by the observation that soap-foam cells exhibit similar size-dependent junctional rea

71 ns (e.g. collagen, elastin) and lipids (e.g. foam cells, extracellular lipids) in the first 200 mum o

72 These findings correlated with decreased foam cell formation (2.27+/-0.57 versus 4.10+/-0.3; P<0.

73 , compared with vehicle control) and reduced foam cell formation (approximately 75%).

74 s a potential mechanism underlying increased foam cell formation and accelerated cardiovascular disea

75 pathways to identify regulators that control foam cell formation and atherogenesis.

76 cholesteryl ester accumulation, resulting in foam cell formation and atherosclerosis progression.

77 ts and is known to be involved in macrophage foam cell formation and atherosclerosis.

78 take in macrophages that would contribute to foam cell formation and atherosclerosis.

79 om macrophages, thereby reducing the risk of foam cell formation and atherosclerosis.

80 droplet protein (LDP), in the regulation of foam cell formation and atherosclerosis.

81 ation antagonizes this program, resulting in foam cell formation and atherosclerosis; however, the mo

82 choline diet-enhanced endogenous macrophage foam cell formation and atherosclerotic lesion developme

83 Macrophage foam cell formation and cholesterol efflux, together wit

84 macrophages may be an important mechanism of foam cell formation and contributor to atherosclerosis d

85 d an M2-predominant phenotype with increased foam cell formation and ER stress.

86 lial cell activation, monocyte accumulation, foam cell formation and expression of pro-inflammatory c

87 Here, we review how foam cell formation and function vary with disease conte

88 at could prevent both lipid accumulation and foam cell formation and further minimise the possible da

89 xtacrine responses associated with increased foam cell formation and inflammatory cytokine elaboratio

90 HLP showed potential in reducing foam cell formation and intracellular lipid accumulation

91 determined by assessing lipid accumulation, foam cell formation and JNK activation in wt, cd9 null a

92 ts engulfment by macrophages, which leads to foam cell formation and lesion development(2,3).

93 phorylated AKT and ERK1/2; exhibited reduced foam cell formation and lipid uptake; and excreted more

94 therosclerosis such as monocyte recruitment, foam cell formation and lipoprotein metabolism.

95 lone had a modest effect on the induction of foam cell formation and only silica was capable of induc

96 -mediated pathway for linked protection from foam cell formation and oxidant stress may have therapeu

97 AR-RGN, a regulatory gene network promoting foam cell formation and risk of CAD.

98 receptor FcepsilonR1-deficient mice, blunted foam cell formation and signaling in IgE-activated macro

99 data reveal novel signaling requirements for foam cell formation and suggest that uptake of distinct

100 Altogether, our findings suggest that foam cell formation and TGF-beta production are driven b

101 In contrast, foam cell formation and TGF-beta production were both dr

102 by oxidized low-density lipoprotein promotes foam cell formation and the progression of atheroscleros

103 ntribution of Vav proteins to CD36-dependent foam cell formation and to identify the mechanisms by wh

104 ogenitor cell expansion and differentiation, foam cell formation and vascular inflammation.

105 hip between ER stress and macrophage-derived foam cell formation and whether ER stress would be invol

106 reviously thought, alternative mechanisms of foam cell formation are now being explored.

107 thways that link innate immune activation to foam cell formation are still poorly identified.

108 scued the suppression of CD36 expression and foam cell formation arising from Plg deficiency.

109 6) accumulate in vivo and mediate macrophage foam cell formation as well as promote platelet hyper-re

110 Foam cell formation because of excessive accumulation of

111 amma in the induction of CD36 expression and foam cell formation by 15(S)-HETE.

112 Next, we investigated foam cell formation by CRP-bound E-LDL.

113 t ANGPTL4 deficiency in macrophages promotes foam cell formation by enhancing CD36 expression and red

114 an M1 phenotype and subsequently suppressed foam cell formation by increasing HDL- and apoA-1-induce

115 ontaining adapter inducing IFN-beta promoted foam cell formation by inducing both NF-kappaB signaling

116 lation into M2 macrophages lead to increased foam cell formation by inducing scavenger receptor CD36

117 1,25(OH)(2)D(3) suppressed foam cell formation by reducing acetylated or oxidized l

118 ctive role during atherosclerosis-associated foam cell formation by signaling through the miR-155-CAR

119 ogenic cytokine TGF-beta inhibits macrophage foam cell formation by suppressing the expression of key

120 al role in CD36 up-regulation, enhancing the foam cell formation by uptaking more ox-LDL.

121 oduction and T cell activation, showing that foam cell formation can occur by immunosuppressive MP.

122 diminished vascular permeability and reduced foam cell formation compared to standard DES in atherosc

123 The Plg-dependent CD36 expression and foam cell formation depended on conversion of Plg to pla

124 Current paradigms of foam cell formation derive from studies of atheroscleros

125 was confirmed as a key factor of neointimal foam cell formation following stent implantation.

126 No role for LKB1 in foam cell formation has previously been reported.

127 These MP also stimulated foam cell formation in a human skin model.

128 diated oxidation, and its ability to prevent foam cell formation in a model for oxidised low density

129 grin activation controls CD36 expression and foam cell formation in alternatively activated monocyte/

130 Reduced foam cell formation in apoE-CD16 DKO mice is not due to

131 n-regulate CD36 expression and CD36-mediated foam cell formation in IL-13-stimulated monocytes/macrop

132 ion of liver X receptor dramatically reduced foam cell formation in macrophages from patients with ty

133 which secrete cytokines that in turn enhance foam cell formation in macrophages.

134 ransgenic animals exhibit reduced macrophage foam cell formation in the arterial wall when these tran

135 Inflammatory processes accompany Mvarphi foam cell formation in the artery wall, yet the relation

136 date the mechanisms by which silica promotes foam cell formation in the lung, and to determine whethe

137 tes reverse cholesterol transport and limits foam cell formation in THP-1 macrophages.

138 fferentiation (CD)36 expression with reduced foam cell formation in TR4(-/-) mice.

139 levels, but the association between SCAP and foam cell formation in vascular smooth muscle cells (VSM

140 uptake of oxidized LDL (oxLDL) in vitro and foam cell formation in vitro and in vivo was significant

141 CD36-dependent uptake of oxLDL in vitro and foam cell formation in vitro and in vivo was significant

142 ration, differentiation into macrophages and foam cell formation in vitro and in vivo.

143 ced uptake of native LDL ex vivo and reduced foam cell formation in vivo, whereas sortilin overexpres

144 cytosis of LDL is a mechanism for macrophage foam cell formation in vivo.

145 umoniae induced IRF3 activation and promoted foam cell formation in wild-type macrophages, whereas th

146 crophages from diabetic patients accelerated foam cell formation induced by modified LDL.

147 We show that ADFP expression facilitates foam cell formation induced by modified lipoproteins in

148 : (i) oxLDL binding to CD36, (ii) macrophage foam cell formation induced by oxLDL, and (iii) platelet

149 ith PPAR-delta agonists was shown to inhibit foam cell formation induced excessive levels of VLDL rem

150 Foam cell formation is a hallmark event during atheroscl

151 nd cellular processes that govern macrophage foam cell formation is critical to understanding the bas

152 In atherogenesis, macrophage foam cell formation is modulated by pathways involving b

153 red cholesterol suggests that the process of foam cell formation is not necessarily detrimental as lo

154 rogenic forms of LDL, but the role of CRP in foam cell formation is unclear.

155 However, it is unclear whether foam cell formation per se protects against atherosclero

156 ing, their role in CD36-dependent macrophage foam cell formation remains unknown.

157 ved that M-CSF itself is capable of inducing foam cell formation similar to that seen in PAP.

158 holesterol accumulation mimicking macrophage foam cell formation that occurs within atherosclerotic p

159 MC1-R confers protection against macrophage foam cell formation through a dual mechanism: It prevent

160 yte/macrophage proinflammatory responses and foam cell formation through coordinated and combined act

161 ence of CD163 in M2-type macrophages-induced foam cell formation through upregulation of CD36 express

162 We conclude that C. pneumoniae facilitates foam cell formation via activation of both MyD88-depende

163 that Vav proteins regulate oxLDL uptake and foam cell formation via calcium- and dynamin 2-dependent

164 protection via heme oxygenase 1 and reduced foam cell formation via liver X receptor, a potent combi

165 Foam cell formation was associated with significant chan

166 Foam cell formation was diminished in FASKOM as compared

167 Neointimal foam cell formation was induced in rabbits (n = 7).

168 C. pneumoniae-induced foam cell formation was significantly reduced by the LXR

169 diet and LDL receptor genotype on macrophage foam cell formation within the peritoneal cavities of mi

170 ficient (Apoe (-/-)) mice by reducing plaque foam cell formation without inflammatory or toxic effect

171 intracellular cholesterol accumulation (ie, foam cell formation) and inflammasome activation, the ex

172 modified low-density lipoprotein uptake and foam cell formation, all of which were abolished by bloc

173 fect of air pollution on 7-KCh accumulation, foam cell formation, and atherosclerosis.

174 rosclerosis, decreased peritoneal macrophage foam cell formation, and downregulated ER stress protein

175 OxLDL uptake, lipid accumulation, foam cell formation, and JNK phosphorylation were partia

176 osphorylated STAT3, interleukin 6 secretion, foam cell formation, and lipid uptake.

177 containing lipoprotein particles, macrophage foam cell formation, and the accelerated atherosclerosis

178 mation, endothelial cell phenotypic changes, foam cell formation, and the expression of CD47 and othe

179 c lipid droplets is a hallmark of macrophage foam cell formation, and the molecular basics involved i

180 n Apoe(-/-) mice led to in vivo increases in foam cell formation, aortic 25-HC levels, and disease pr

181 t that is critical for lipid degradation and foam cell formation, as occurs in atherosclerosis.

182 ation, endothelial cell function, macrophage foam cell formation, as well as insulin secretion from p

183 ake of OxLDL by macrophage SR contributes to foam cell formation, but the importance of this pathway

184 ng cascades that are required for macrophage foam cell formation, but the mechanisms by which CD36 si

185 oxidized low density lipoprotein uptake, and foam cell formation, critical events underlying the path

186 ve the capacity to regulate inflammation and foam cell formation, pathological angiogenesis and calci

187 neutralizing and clearing OSE and preventing foam cell formation, suggesting similar applications in

188 aining plasma lipoproteins lead to increased foam cell formation, the first step in the development o

189 butions of lipid uptake and TLR signaling in foam cell formation, we established an in vitro assay us

190 3-induced CD36 expression and CD36-dependent foam cell formation, whereas13(S) Hydroperoxyoctadecadie

191 We found that lipid-containing MP promoted foam cell formation, which was enhanced by TLR stimulati

192 157 reduces monocyte accumulation and blocks foam cell formation.

193 ol LDLR(-/-) mice, using an in vivo model of foam cell formation.

194 ophages resulted in increased LDL uptake and foam cell formation.

195 rosis and we demonstrated a role for 25HC in foam cell formation.

196 onses to inflammatory signals, and increased foam cell formation.

197 ar function, reduce inflammation and inhibit foam cell formation.

198 is, centered on the regulation of macrophage foam cell formation.

199 had decreased CD36 expression and diminished foam cell formation.

200 otal role of plasminogen (Plg) in regulating foam cell formation.

201 sterol ester accumulation in macrophages and foam cell formation.

202 IFN-alpha to TLR2 activator promoted robust foam cell formation.

203 ogenous microparticles (MP) to contribute to foam cell formation.

204 tivation of multiple distinct TLR can induce foam cell formation.

205 ansport in macrophages, which contributes to foam cell formation.

206 aintaining chronic inflammation and inducing foam cell formation.

207 roliferator-activated receptor alpha blocked foam cell formation.

208 vel macrophage subset that is protected from foam cell formation.

209 droxycholesterol (25-HC) promotes macrophage foam cell formation.

210 ted that the TF ATF3 may regulate macrophage foam cell formation.

211 o not induce IFN, like TLR2, did not enhance foam cell formation.

212 a signaling pathway required for macrophage foam cell formation.

213 protein expression, as well as CD36-related foam cell formation.

214 y which Vav proteins regulate CD36-dependent foam cell formation.

215 nted macrophage cholesterol accumulation and foam cell formation.

216 ificantly blocked oxLDL uptake and inhibited foam cell formation.

217 l as enhanced cholesterol efflux and reduced foam cell formation.

218 lipid bodies in macrophages and consequently foam cell formation.

219 MAC mediated endothelial damage and promoted foam cell formation.

220 CD36 expression with decreased or increased foam cell formation.

221 down macrophage cells reversed the decreased foam cell formation.

222 development of atherosclerosis is macrophage foam cell formation.

223 ce or absence of oxidized LDL, then measured foam cell formation.

224 ux and hence play a vital role in macrophage foam cell formation.

225 or IRF3, but not TLR3, significantly reduced foam cell formation.

226 rs to be a relatively pure model of impaired foam cell formation.

227 cholesterol efflux, and increased macrophage foam cell formation.

228 es monocyte differentiation, activation, and foam cell formation.

229 ich is a counterregulatory mechanism against foam cell formation.

230 rotein (oxLDL) by macrophages (Mvarphis) and foam cell formation.

231 stablish the role of LKB1 in atherosclerotic foam cell formation.

232 signaling pathway controlling CD36-mediated foam cell formation/cardiovascular diseases, and finding

233 Thus, macrophage Hilpda is crucial to foam-cell formation and lipid deposition, and to control

234 cing atherosclerosis progression by inducing foam-cell formation, metabolic adaptation of infiltrated

235 Interestingly, Mcl-1(-/-) peritoneal foam cells formed up to 45% more multinucleated giant ce

236 show that MafB is predominantly expressed in foam cells found within atherosclerotic lesions, where M

237 D68(+), primarily macrophages and macrophage foam cells) from plaques.

238 leukocyte accumulation, lipid accumulation, foam cell generation and endothelial cell injury were al

239 mice reduces the number of lipid droplets in foam cells in atherosclerotic lesions and protects the m

240 of SMPDL3A by cholesterol-loaded macrophage foam cells in lesions may decrease local concentrations

241 ein Nef causes dyslipidemia and formation of foam cells in mouse models of atherosclerosis.

242 Although Mac(AIR) comprise the earliest foam cells in plaques, their proliferation during plaque

243 otein degradation and uptake into macrophage foam cells in the arterial intima.

244 promotes cholesterol efflux from macrophage foam cells in the arterial wall.

245 y accepting free cholesterol from macrophage foam cells in the artery wall.

246 subsequent accumulation of leukocyte-derived foam cells in the artery wall.

247 iltration, thereby stimulating regression of foam cells in the artery.

248 D68+ macrophages, including lipid-containing foam cells, in atherosclerotic lesions in the aortic arc

249 ulture of large SMCs with macrophage-derived foam cells induced a transition to the small phenotype w

250 Foam cell infiltration was responsible for 70% of false

251 ages, with ensuing formation of lipid-filled foam cells, initiate atherosclerotic lesion formation, a

252 ferentiation of macrophages into lipid-laden foam cells is central to the development of atherosclero

253 cholesterol efflux capacity from macrophage foam cells is not associated with cardiovascular or all-

254 age phenotype, but how this is controlled in foam cells is not known.

255 erogenesis because their transformation into foam cells is responsible for deposition of lipids in pl

256 accumulation and the consequent formation of foam cell-like cells in adipose tissue.

257 mor necrosis factor) expression as well as a foam cell-like population expressing TREM2 (triggering r

258 Macrophages, DCs, foam cells, lymphocytes, and other inflammatory cells ar

259 n mediating cellular cholesterol efflux from foam cell macrophages and to identify the cellular chole

260 Cholesterol-loaded foam cell macrophages are prominent in atherosclerotic l

261 emplified by the requirement of lipid-laden, foam cell macrophages for atherosclerotic lesion formati

262 phenotypes, including phenotypes resembling foam cells, macrophages, mesenchymal stem cells and oste

263 the function of CRP to prevent formation of foam cells may influence the process of atherogenesis.

264 s affected cholesterol-ester accumulation in foam cells of the THP1 monocytic cell line.

265 to recovery of vasoactivity, but not loss of foam cells or recovery of permeability, while pretreatme

266 ine consistent marker sets for the different foam cell phenotypes in experimental animals and humans.

267 e relative contribution of SMCs to the total foam cell population and their expression of ABCA1 in co

268 smooth muscle cells (SMCs) contribute to the foam cell population in arterial plaque, and express low

269 rogression of macrophages to the lipid-laden foam cells present in atherosclerotic plaques.

270 Macrophage-derived foam cells promote selective migration from the media of

271 mation of lipid-laden macrophages, known as "foam cells." Recently, we reported that CD36, a scavenge

272 nd the SMC-specific marker SM alpha-actin of foam cell-rich lesions revealed that 50+/-7% (average+/-

273 LDL in the presence of C1q alters macrophage foam cell survival or function.

274 efferocytotic removal of apoptotic cells and foam cells sustains lesion progression.

275 /-)LDLR(-/-) mice develop significantly more foam cells than control LDLR(-/-) mice, using an in vivo

276 -rich lipoprotein particles, and evolve into foam cells that form components of vulnerable atheroscle

277 BM cleaves CD36 and reduced the formation of foam cells, the hallmark of M. tuberculosis infection.

278 Oxidized lipoproteins convert macrophages to foam cells through lipid uptake and TLR signaling.

279 Foam cell transformation of lipid-laden THP-1 macrophage

280 t decrease of endothelial cell junctions and foam cell transformation of monocytes, confirming the re

281 y role in IFN-gamma-induced inflammation and foam cell transformation, a better understanding of the

282 tivation and thereby regulates macrophage to foam cell transformation.

283 were dramatically suppressed in lipid-laden foam cells treated with IL10.

284 Foam cells undergo apoptosis and, if not efficiently cle

285 Macrophages transform into foam cells upon taking-in lipids.

286 in eliminating the activity of E-LDL to form foam cells was not impaired by the presence of PEt.

287 them, we found that the level of miR-155 in foam cells was the most significantly elevated in a dose

288 is in vitro model of cholestryl ester-loaded foam cells was then used for experimental validation.

289 sistent with previous reports, we found that foam cells were markedly increased in the lungs of patie

290 he diseased portion, only macrophage-derived foam cells were retrieved.

291 d error of the mean, n=14 subjects) of total foam cells were SMC derived.

292 bility to take up lipids and to develop into foam cells when exposed to modified low-density lipoprot

293 ated the caspase-3 and caspase-8 pathways in foam cells, which is responsible for the switch from nec

294 as quantified by incubating human macrophage foam cells with apoB-depleted serum.

295 ntified using incubation of human macrophage foam cells with apolipoprotein B-depleted plasma.

296 ntified using incubation of human macrophage foam cells with apolipoprotein B-depleted plasma.

297 internalize modified lipids, and convert to foam cells with diseased phenotypes.

298 Treatments of these foam cells with ritonavir, nelfinavir, and saquinavir at

299 after SCI, macrophages are best described as foam cells, with lipid catabolism representing the main

300 after SCI, macrophages are best described as foam cells, with lipid catabolism representing the main